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Figure 3 | Acta Neuropathologica Communications

Figure 3

From: Obesity and diabetes cause cognitive dysfunction in the absence of accelerated β-amyloid deposition in a novel murine model of mixed or vascular dementia

Figure 3

Aβ is not deposited in the vasculature. Large numbers of activated astrocytes could be seen both around amyloid cores and around some larger blood vessels (arrowheads) in older db/AD mice (a) There was no significant co-staining of amyloid and collagen IV, indicating that Aβ was not deposited in blood vessels. Red: GFAP, Green: Collagen IV, Blue: Amylo-Glo. db/AD mice did not have significantly more Aβ40 (b) or Aβ42 (c) in plasma, compared with AD mice (n = 18 F WT; 18 F db; 14 F AD; 13 F db/AD: 7–12 months old: p > 0.06), though mice containing the AD mutations had significantly more than those without (p ≤ 0.0001 for AD overall). Though the activities were significantly different in mice homozygous for the db mutation, neprilysin (d; p < 0.02) and insulin degrading enzyme (IDE: e; p < 0.003) activities were not increased relative to db WT mice (1–4 months old: n = 5 F/7 M Lepr +/+; 8 F/4 M Lepr db/db; 6 F/6 M Lepr db/+). Endothelin converting enzyme (ECE1: f) protein expression was unaffected by the db (p < 0.65) and AD (p > 0.1) genotypes (7–12 months old: n = 14 F/7 M WT; 16 F/5 M db; 12 F/5 M AD; 12 F/6 M db/AD). Similarly ECE1 (g) and ECE2 (not shown) mRNA expression was unchanged in diabetic mice (p > 0.38 for the db genotype overall), though ECE1 expression was reduced in AD mice relative to WT (* = p < 0.03: n = 1 F/4 M WT; 2 F/4 M db; 1 F/3 M AD; 1 F/3 M db/AD).

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